Impaired fasting glucose and impaired glucose tolerance in urban population in India.

AIMS: To study prevalence of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in urban Indians and their demographic and anthropometric characteristics. METHODS: Data on capillary blood glucose (OGTT), anthropometric and demography details were available in 10 025 subjects (M : F 4711 : 5314) aged > or = 20 years. Glucose tolerance was categorized as normal, isolated IFG, isolated IGT, IFG + IGT and diabetes using the fasting and 2-h blood glucose (2hBG; 75-g glucose load) values. Subjects with known diabetes were excluded. RESULTS: Age-standardized prevalences of IFG, IGT and newly detected diabetes were 8.7%, 8.1% and 13.9%, respectively. IFG was more prevalent in women (9.8%) than in men (7.4%) (chi2 = 13.62, P = 0.0002), while the gender differences in IGT (men 8.4%, women 7.9%) and diabetes (men 13.3%, women 14.3%) were not significant. Body mass index and waist circumference were higher in glucose-intolerant groups than in normal glucose tolerance (NGT). Prevalence of diabetes, IGT and IFG + IGT increased with age. Among the IFG, 4% had diabetes and 27.1% had IGT using 2hBG criteria. In IFG, the fasting and 2hBG values were not correlated. CONCLUSIONS: Prevalences of IFG and IGT were similar in urban Indians and an overlap occurred in only less than half of these subjects. IFG was more common in women. Subjects with IFG were older and had more adverse anthropometric characteristics in comparison with NGT. IFG did not show an increasing trend with age.     

空腹血糖异常人群胰岛素分泌功能及胰岛素抵抗状态的探讨

目的　探讨空腹血糖异常人群的胰岛素分泌及胰岛素抵抗状态。　方法　选择包钢糖尿病普查中复查口服葡萄糖耐量试验 (OGTT) 3985例 ,分为 6组 :正常糖耐量 (NGT)组 2 5 88例 ,异常空腹血糖 (IFG)组 2 72例 ,糖耐量减低 (IGT)组 4 4 9例 ,空腹血糖异常伴糖耐量减低 (IFG/ IGT)组116例 ,新诊断糖尿病 (DM1)组 338例 ,已知糖尿病 (DM2 )组 2 2 2例。测腰围、体重指数、血压、血脂及血浆胰岛素 ,应用稳态模式胰岛素抵抗指数 (HOMA- IR)作为胰岛素抵抗指标 ,稳态模式胰岛 β细胞功能指数 (HBCI)及胰岛素分泌指数 (IS)作为胰岛素分泌指标 ,并对 6组患者的这些指标及临床特征 ,进行对比分析。　结果　与 NGT组比较 ,IFG组 HOMA- IR(1.4 6± 0 .6 0 ,1.0 6± 0 .6 4 ,t=- 6 .716 ,P<0 .0 0 1)、空腹胰岛素 (FINS) (17.90± 10 .0 6 ,15 .79± 10 .94 ,t=- 2 .0 71,P=0 .0 39)增高 ,HB-CI(4.6 5± 0 .6 0 ,5 .2 7± 0 .76 ,t=3.399,P<0 .0 0 1)及 IS(0 .86± 0 .6 0 ,0 .99± 0 .6 2 ,t=2 .36 6 ,p=0 .0 18)降低 ;IGT组 HOMA- IR(1.39± 0 .5 8,t=4 .6 98) ,FINS(2 1.2 7± 15 .39,t=4 .4 93)、2 - h胰岛素(6 0 .84± 37.86 ,t=8.4 82 )、HBCI(5 .4 7± 0 .79,t=2 .6 98)、IS(1.2 5± 0 .6 1,t=4 .0 34,P值均 <0     

Decreased insulin action and insulin secretion predict the development of impaired glucose tolerance

Summary The relative importance of insulin resistance and abnormal insulin secretion as risk factors for the development of impaired glucose tolerance (IGT) is controversial. Few prospective data are available on metabolic precursors of IGT. We examined the relation of fasting serum insulin level (as a marker of insulin resistance) and change in insulin/glucose ratio (ΔI ₃₀/ΔG₃₀) over the first 30 min after glucose ingestion (as a marker of insulin secretion) as predictors of the 7-year development of IGT in 839 Mexican Americans and non-Hispanic whites with normal glucose tolerance at baseline from the San Antonio Heart Study. IGT eventually developed in 148 subjects. When modelled separately, fasting serum insulin (odds ratio (OR)=2.60,95 % confidence interval (CI)=1.58,4.28,p<0.005), but not ΔI ₃₀/ΔG₃₀ (OR=0.80, 95 % CI=0.50,1.27,p=0.339) predicted the development of IGT. However, when both variables were included in the same logistic regression model, fasting serum insulin (OR=3.50, 95 % CI=1.97,6.21,p<0.001) and low ΔI ₃₀/ΔG₃₀ (OR=0.48, 95 % CI=0.28,0.82,p=0.008) both predicted IGT. These results were basically unchanged after further adjustment for obesity, body fat distribution and fasting plasma glucose level. We conclude that both decreased insulin secretion (as assessed by low ΔI ₃₀/ΔG₃₀) and increased insulin resistance (as assessed by fasting serum insulin) predict the development of IGT and are thus early precursors of non-insulin-dependent diabetes mellitus; further studies of insulin secretion should take into account the level of basal insulin resistance.     

糖调节受损个体胰岛β细胞功能和胰岛素抵抗观察

评价152例人选者[正常糖耐量、空腹血糖受损和(或)糖耐量受损]胰岛β细胞功能和胰岛素抵抗.结果 显示空腹血糖受损者主要表现胰岛素早期分泌功能缺陷和基础分泌不足,胰岛素抵抗严重;糖耐量受损者则胰岛素早期和晚期分泌功能显著下降伴轻度胰岛素抵抗.     

空腹血糖受损并糖耐量受损患者血管内皮功能及代谢功能观察

目的：观察空腹血糖受损并糖耐量受损（ IFG＋IGT）患者血管内皮功能及代谢功能情况。方法选择IFG＋IGT者72例（ E组）,其中非肥胖30例（ E1组）,肥胖42例（ E2组）;另选择糖耐量正常的健康人群142例（ N组）,其中非肥胖75例（ N1组）、肥胖67例（ N2组）。做口服葡萄糖耐量试验及胰岛素释放试验检测血糖、免疫活性胰岛素,同时检测空腹血脂、游离脂肪酸、脂联素。采用免疫比浊法检测超敏C反应蛋白（ hs-CRP）,RIA法检测血清内皮素（ SET）。留取晨尿,采用未抽提法测定内皮素（ UET）,散射比浊法检测尿微量白蛋白（ MUA）。观察血压和腰围。彩超测定肱动脉休息时、加压及服用硝酸甘油后的内径变化,计算内皮依赖性血管舒张功能（ EDD）及内皮非依赖性血管舒张功能（ EID）指标（ΔD％、ΔD1％）。结果校正性别、年龄后,E和N组比较、E2与N2组比较及E1与N1组比较,MUA、hs-CRP、UET、SET、ΔD％、ΔD1％差异有统计学意义（P均＜0．05）;N2与N1组比较hs-CRP、UET和SET差异有统计学意义（P均＜0．05）;E2与E1组比较MUA、hs-CRP、UET和SET差异有统计学意义（P均＜0．05）。结论 IFG＋IGT患者大血管和微血管内皮功能均出现异常,尤以肥胖者为著;患者的代谢功能亦出现异常,主要表现为高血压、高血糖、脂代谢紊乱、胰岛素抵抗及胰岛分泌功能下降。     

红细胞体积分布宽度与糖代谢异常/糖耐量异常和糖尿病相关

目的探讨红细胞体积分布宽度（RDW）与2型糖尿病（T2DM）、空腹血糖受损／葡萄糖耐量异常（IFG／IGT）的相互关系。方法对152例在我院定期进行健康体检或治疗的患者,依据血糖情况分为3组,其中T2DM组42例,IFG／IGT组38例,正常对照（NGT）组72例,采取空腹血,采用全自动血液分析仪测定RDW、血红蛋白,多功能血生化自动分析仪测定血总胆固醇、三酰甘油、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、血肌酐、血尿素氮和空腹血糖,同时统计高血压、冠心病的发病率并分析其关系。结果RDW在T2DM组、IFG／IGT组和NGT组之间比较具有统计学差异,其中T2DM组和NGT组、IFG／IGT组比较,差异均有统计学意义（P〈0．05或P〈0．01）,IFG／IGT组与NGT组比较差异无统计学意义（P〉0．05）。多因素直线回归分析显示空腹血糖（P〈0．01）和高密度脂蛋白胆固醇（P〈0．05）是RDW的独立危险因子。结论T2DM患者RDW升高,RDW的变化与空腹血糖水平相关。     

Impact of lowering the criterion for impaired fasting glucose on identification of individuals with insulin resistance. The GISIR database

OBJECTIVE: We assessed the accuracy of the American Diabetes Association (ADA)2003 definition of impaired fasting glucose (IFG) in identifying subjects with low insulin sensitivity, and determined cardiovascular risk factors in ADA2003 IFG subjects. RESEARCH DESIGN AND METHODS: This study included 930 non-diabetic Italian Caucasians from the GISIR database in which subjects underwent a hyperinsulinaemic-euglycaemic clamp performed with a standard technique. Low insulin sensitivity was defined as being in the lower quartile of glucose metabolized during the last hour of the clamp (M). Subjects were stratified in the following groups: normal fasting glucose (NFG) (<100 mg/dL), IFG100 (100-109 mg/dL), ADA1997 IFG110 (110-125 mg/dL), and ADA2003 IFG (100-125 mg/dL). RESULTS: The sensitivity of identifying subjects with low insulin sensitivity increased adopting the ADA2003 criterion. After Bonferroni correction for multiple comparisons, both IFG100 and ADA1997 IFG110 showed significantly higher body mass index (BMI), waist, systolic blood pressure (SBP) and diastolic blood pressure (DBP), triglyceride, fasting plasma insulin (FPI) and fasting plasma glucose (FPG), and lower insulin sensitivity as compared with NFG. As compared with IFG100, ADA1997 IFG110 showed significantly higher BMI, waist, SBP, FPI, FPG, and lower insulin sensitivity. ADA2003 IFG group showed significantly higher BMI, waist, SBP and DBP, triglyceride, cholesterol, FPI, and FPG, but lower HDL levels and insulin sensitivity compared with NFG subjects. CONCLUSIONS: Although neither the ADA2003 nor the ADA1997 definition of IFG appears to be particularly efficacious for the identification of subjects' low insulin sensitivity, lowering the criterion to the ADA2003 glucose threshold increased the sensitivity without affecting the specificity. ADA2003 IFG showed a worse cardiovascular risk profile compared with NFG.     

空腹血糖异常、糖耐量减低患者血清胰岛素水平的变化及其意义

目的 观察空腹血糖异常(IFG)、糖耐量减低(IGT)患者血清胰岛素水平的变化。方法 对50例空腹血糖和糖耐量正常者(NGT)、40例IFC和80例IGT患者行口服葡萄糖耐量试验(0GTT)，用氧化酶法检测血糖，用放免法测定血清空腹及餐后2小时胰岛素。结果 IFG、IGT组空腹血糖、空腹胰岛素水平及胰岛素敏感指数较NGT组明显升高(P＜0.05或P＜0．01)，IFG组胰岛素敏感指数与IGT组比较无显著性差异(P＞0．05)。结论 在IFG、IGT状态下已经存在胰岛素抵抗，而且在程度上两者间并没有显著性差异，应早期干预治疗。     

Peripheral and hepatic insulin sensitivity in subjects with impaired glucose tolerance

Summary Recent evidence suggests that the post-prandial hyperglycaemia in impaired glucose tolerance is primarily due to impaired suppression of basal hepatic glucose output. This in turn appears to be secondary to decreased first phase insulin secretion, although decreased hepatic insulin sensitivity, which is a feature of non-insulin-dependent diabetes mellitus, might also play a role. Eight mildly overweight subjects with impaired glucose tolerance and eight closely matched control subjects with normal glucose tolerance underwent an intravenous glucose tolerance test to assess first phase insulin secretion. Insulin sensitivity was examined by a 150-min hyperinsulinaemic-euglycaemic clamp. Somatostatin was infused from 150 min to suppress endogenous insulin secretion, and glucagon and insulin were replaced by constant infusion. Glucose with added dideuterated glucose (labelled infusion technique) was infused to maintain euglycaemia. First phase insulin secretion ( 0–10 min insulin area ÷ 0–10 min glucose area) was significantly decreased in the subjects with impaired glucose tolerance (median [range]: 1.2 [0.2–19.4] vs 9.1 [2.6–14.5] mU·mmol^–1; p<0.01). During the clamp, circulating insulin (93±8 [mean±SEM] and 81±10 mU·l^–1) and glucagon (54±4 and 44±6 ng·l^–1) levels were comparable. Total glucose disposal was decreased in subjects with impaired glucose tolerance (2.78±0.27 vs 4.47±0.53 mg·kg^–1·min^–1; p<0.02), and was primarily due to decreased non-oxidative glucose disposal. However, hepatic glucose output rates were comparable during the clamp (0.38±0.10 and 0.30±0.18 mg·kg^–1·min^–1). Therefore, the main defects in subjects with impaired glucose tolerance are decreased first phase insulin secretion and peripheral non-oxidative glucose disposal, but hepatic glucose output shows normal responsiveness to insulin.Abbreviations FPIS First phase insulin secretion - PG plasma glucose - NIDDM non-insulin-dependent diabetes mellitus - IGT impaired glucose tolerance - HGO hepatic glucose output - IVGTT intravenous glucose tolerance test - OGTT oral glucose tolerance test     

新疆汉、维民族糖调节受损人群胰岛素分泌功能和胰岛素作用功能的研究

目的 评估新疆汉、维民族在IFG,IGT及IGR阶段的胰岛素分泌功能和胰岛素作用功能。 方法 采用多中心研究进行横断面调查,行OGTT试验。用胰岛素抵抗指数（HOMA-IR）评估IR,胰岛β细胞功能指数（HOMA-β）评估基础胰岛素分泌;ΔI30/ΔG30评价胰岛素早相分泌,ΔI30/ΔG30/HOMA-IR评估葡萄糖处置指数（DI）。 结果 WC、BMI、血脂、FIns、2 hIns在汉、维民族不同糖代谢组差异有统计学意义。IFG组与NGT、IGT组比较,汉、维族人群的HOMA-IR差异有统计学意义。在汉族中NGT组与IGT、IGR组比较,HOMA-β差异有统计学意义（P=0.030、0.044）,而在维族只有IFG组与NGT组比较差异有统计学意义（P=0.001）。ΔI30/ΔG30、DI在两民族不同糖代谢组差异均无统计学意义。 结论 汉族人群IR在IFG阶段,胰岛素分泌功能在IGT阶段起主要作用。IR和胰岛素分泌功能在维族人群IFG阶段起重要作用。胰岛素早相分泌及葡萄糖处置功能在糖调节受损阶段作用不显著。     

上海地区肥胖糖调节受损者的胰岛素敏感性和1相胰岛素分泌功能研究

目的研究上海地区肥胖的糖调节受损(IGR)者胰岛素敏感性和胰岛β细胞1相胰岛素分泌功能。方法共有129例受试者[非肥胖正常对照38名,IGR包括单独糖耐量受损(IGT)64例,单独空腹血糖受损(IFG)8例,IFG+IGT 19例]接受了口服75g葡萄糖耐量试验和胰岛素改良的减少样本数(n =12)的Bergman微小模型技术结合频繁采血的静脉葡萄糖耐量试验(FSIGTT)。胰岛素抵抗由FSIGTT中胰岛素敏感性指数(S1)加以评估,而FSIGTT中对葡萄糖急性胰岛素分泌反应(AIRg)则用以评价胰岛β细胞分泌功能。处理指数(DI=AIRg×S1)用于评价AIRg是否代偿机体的胰岛素抵抗。结果(1)与正常对照组相比,3组IGR患者之S1明显降低(均P<0．01),3组差异无统计学意义;(2)AIRg在正常组和IGT组之间差异无统计学意义,但均大于IFG和IFG+IGT组,差异有统计学意义(P<0．05或JP<0．01)。IFG +IGT组的AIRg值显著低于IGT组(P<0．01);(3)与正常组相比,DI指数在3组IGR显著降低(P< 0．01),但在IGR组间差异无统计学意义;(4)S1与空腹胰岛素、体重指数、血清尿酸呈显著负相关(校正r2 =0．568,P<0．01);而AIRg与2h胰岛素显著正相关,与空腹血糖、2h血糖和年龄负相关(校正r2=0．402, P<0．01)。结论上海地区肥胖的初诊IGR患者(包括单独IGT、单独IFG和IFG+IGT患者)存在着程度近似的胰岛素抵抗;急性相胰岛素分泌功能在校正胰岛素抵抗影响因素后IGT患者尚属正常,在IFG和IFG+IGT患者已明显降低,且3组的β细胞代偿功能均为一致性失代偿。     

空腹血糖受损与糖耐量受损患者血管内皮功能的对比研究

目的:应用多普勒超声技术检测空腹血糖受损(IFG)与糖耐量受损(IGT)患者的血管内皮功能,探讨其对动脉粥样硬化的影响。方法:根据口服葡萄糖耐量试验(OGTT)结果,选择血糖正常(NGT)组25例,IFG组24例,IGT组22例,检测TC、TG、LDL-C、HDL-C、空腹血糖(FPG)、空腹胰岛素(FINS)、糖化血红蛋白(HbA1C)、高敏C反应蛋白(hs-CRP)及血管性血友病因子(vWF),OGTT后2h血糖(2hPG)及2h胰岛素(2hINS),以及肱动脉内皮依赖性舒张功能(EDD)。结果:IGT组vWF较IFG组、NGT组明显升高[(170.25±21.76)%∶(155.16±17.19)%、(135.46±15.52)%,P<0.05～0.01],肱动脉EDD较IFG组、NGT组明显降低[(4.86±0.94)%∶(5.47±0.90)%、(6.24±0.97)%,P<0.05～0.01];IFG组vWF较NGT组明显升高[(155.16±17.19)%∶(135.46±15.52)%,P<0.05],肱动脉EDD较NGT组明显降低[(5.47±0.90)%∶(6.24±0.97)%,P<0.05]。多因素逐步回归分析显示,EDD与2hPG、LDL-C明显负相关(r分别为-0.73、-0.59,P<0.05)。结论:IGT较IFG对血管内皮功能危害更大,加强IGT防治对延缓动脉粥样硬化更为重要。     

肥胖和非肥胖糖耐量受损患者胰岛素敏感性和1相胰岛素分泌研究

目的研究肥胖和非肥胖糖耐量受损(IGT)患者的胰岛素敏感性和β细胞1相胰岛素分泌功能,以探讨在IGT患者中肥胖对胰岛素抵抗和1相胰岛素分泌的影响。方法共有99位受试者(包括正常对照者32名,肥胖IGT44例,非肥胖IGT23例)接受了口服75 g葡萄糖耐量试验(OGTT)和胰岛素改良的减少样本数(采血样12次)的Bergman微小模型技术结合静脉葡萄糖耐量试验(FSIGTT)。胰岛素抵抗由FSIGTT中胰岛素敏感性指数(SI)加以评估,而OGTT中糖负荷后30 min胰岛素增值与血糖增值之比值[ΔI30/ΔG30=(I30 min-I0 min) /(G30 min-G0 min)]和FSIGTT中急性胰岛素分泌反应(AIRg)则用以评价胰岛β细胞分泌功能。处理指数(DI =AIRg×SI)用于评价AIRg是否代偿机体的胰岛素抵抗。结果与正常对照组[(7.52±10.89)×10-4]相比,二组IGT患者之SI明显降低,而肥胖IGT组的SI[(1.72±1.11)×10-4]较非肥胖组[(3.15±1.49)×10-4]更低(均P<0.01); AIRg和ΔI30/ΔG30在正常组(412±191,14.45±8.47)和肥胖IGT组(378±235,17.02±11.30)之间差异无统计学意义,但均大于非肥胖组(196±160,8.93±6.69,均P<0.01);与正常组(2 851±1 180)相比,DI指数在二组IGT显著降低(595±485,584±517),但后二组间此值差异无统计学意义。SI与2 h胰岛素、体重指数、尿酸和胆固醇呈显著的负相关性(校正r2=0.603,P<0.01);而AIRg与ΔI30/ΔG30显著正相关,与空腹血糖负相关(校正r2=0.479,P<0.01)。结论IGT患者存在胰岛素抵抗和β细胞功能异常。与非肥胖IGT患者相比,肥胖IGT患者胰岛素抵抗程度更为严重,但胰岛β细胞胰岛素1相分泌相对充分。     

Early insulin secretion failure leads to diabetes in Chinese subjects with impaired glucose regulation

Background Both beta‐cell dysfunction and decreased insulin sensitivity are involved in the pathogenesis of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG), while their relative contribution in the progression to type 2 diabetes still remains controversial. The aim of the present study is to clarify this process in Chinese subjects by using cross‐sectional method. Methods 2975 Chinese subjects were classified into: normal glucose tolerance (NGT), impaired glucose regulations (IGR), and diabetes mellitus (DM) based on oral glucose tolerance test (OGTT). The IGR group was sub‐classified as isolated IFG, isolated IGT and combined glucose intolerance (CGI). The DM group was sub‐classified as normal fasting plasma glucose and 2‐hour hyperglycemia (N0D2), fasting hyperglycemia and normal 2‐hour plasma glucose (D0N2), and both fasting and 2‐hour hyperglycemia (D0D2). Results As far as insulinogenic index (IGI) was concerned, there was no difference between IFG and IGT in either gender, however, HOMA2‐B% (homeostasis model assessment for beta‐cell function) of IGT was higher than that of IFG and CGI in both male and female (P < 0.05). In the diabetic sub‐groups, IGI of N0D2 was higher than that of D0N2, and both deteriorated compared with those of IGT and IFG, respectively. HOMA2‐B% of N0D2 was still higher than that of D0N2 and D0D2. No significant difference was detected in OGIS and HOMA2‐S% (homeostasis model assessment for insulin sensitivity) between IFG and IGT, and this was the case between N0D2 and D0N2. OGIS and HOMA‐IR of IGR sub‐groups were not different from those of their diabetic counterparts. Conclusion Failure of beta‐cell function might be the main reason for both IGT and IFG developing into diabetes instead of aggravated insulin resistance. Copyright © 2008 John Wiley & Sons, Ltd.     

Rosiglitazone improves insulin sensitivity, glucose tolerance and ambulatory blood pressure in subjects with impaired glucose tolerance.

AIMS: To determine the effects of rosiglitazone on insulin sensitivity, glucose tolerance and ambulatory blood pressure when administered to subjects with persistent impaired glucose tolerance (IGT). METHODS: Eighteen subjects with persistent IGT were randomized to receive rosiglitazone 4 mg twice daily or matching placebo for 12 weeks. Evaluation at baseline and at the end of treatment included measurement of whole body insulin sensitivity during a euglycaemic hyperinsulinaemic clamp and deriving an insulin sensitivity index. Changes in glucose and insulin concentration were determined after oral glucose tolerance test (OGTT) and mixed meal tolerance tests, and 24-h ambulatory blood pressure was monitored. RESULTS: Rosiglitazone significantly improved the insulin sensitivity index by 2.26 micro g/kg per min per pmol/l relative to placebo (P = 0.0003). Four of nine subjects receiving rosiglitazone reverted to normal glucose tolerance and 5/9 remained IGT, although four of these had improved 2-h glucose values. In the placebo group, 1/9 subjects progressed to Type 2 diabetes and 8/9 remained IGT. Following OGTT and meal tolerance test, glucose and insulin area under curve were reduced over 3 and 4 h, respectively. Compared with placebo, ambulatory blood pressure decreased significantly in the rosiglitazone group by 10 mmHg systolic (P = 0.0066) and 8 mmHg diastolic (P = 0.0126). CONCLUSIONS: Consistent with its effects in patients with Type 2 diabetes, rosiglitazone substantially improved whole body insulin sensitivity and the glycaemic and insulinaemic responses to an OGTT and meal tolerance test in subjects with persistent IGT. Furthermore, rosiglitazone reduced systolic and diastolic ambulatory blood pressure in these subjects.     

空腹血糖受损与糖耐量减低的概念及表现谱的差异和对策

1997年美国糖尿病学会(ADA)提出空腹血糖受损(IFG)的概念,2003年11月ADA提出IFG下限诊断标准从6.1mmol/L下调到5.6mmol/L。IFG与糖耐量减低(IGT)人群进展为2型糖尿病的危险均较正常血糖人群高,但两者的表现谱却存在许多差异,如两者的患病率具有性别及种族差异;胰岛素分泌及胰岛素抵抗状况也不同;两者与血管病变的关系及血管病变的发生率和病死率也有差异。因此,基于IFG、IGT的病理生理学应对其采取相应的干预措施。     

Insulin secretory responses to rising and falling glucose concentrations are delayed in subjects with impaired glucose tolerance

Aims/hypothesis. We hypothesized that beta-cell responses to changes in glucose would not be normal in subjects with impaired glucose tolerance (IGT). Methods. Three groups of 6 subjects were studied: normal weight with normal glucose tolerance (control subjects); obese with normal glucose tolerance (Obese-NGT); and obese with IGT (Obese-IGT). All subjects had a graded glucose infusion protocol to increase (step-up) and then decrease (step-down) plasma glucose. We obtained average insulin-secretion rates (ISR) over the glucose range common to all three groups during step-up and step-down phases, minimal model indices of beta-cell function (f_b, f_d, f_s, T_up, T_down ), and insulin sensitivity (Si). Results. ISR differed significantly between step-up and -down phases only in Obese-IGT individuals. Basal (f_b) and stimulated (f_d, f_s) beta-cell sensitivity to glucose were similar in the three groups. Delays between glucose stimulus and beta-cell response during both step-up (T_up) and -down (T_down) phases were higher in Obese-IGT compared to Controls and Obese-NGT individuals. The product ISR × Si (10^–5·min^–2× l) was lower in Obese-IGT compared to Controls, both during step-up (919 ± 851 vs 3192 ± 1185, p < 0.05) and step-down (1455 ± 1203 vs 3625 ± 691, p < 0.05) phases. Consistently, the product f_s× Si (10^–14·min^–2· pmol^–1× l) was lower in Obese-IGT than in control subjects (27.6 ± 25.4 vs 103.1 ± 20.2, p < 0.05). Conclusion/interpretation. Subjects with IGT are not able to secrete insulin to compensate adequately for insulin resistance. They also show delays in the timing of the beta-cell response to glucose when glucose levels are either rising or falling. [Diabetologia (2002) 45: ▪–▪] Received: 30 July 2001 and in revised form: 21 November 2001     

Impaired glucose tolerance and fasting hyperglycaemia have different characteristics.

AIMS: Use of the oral glucose tolerance test (OGTT) to define glucose intolerance in the general population may bias towards selection of those with insulin resistance. Beta cell function and insulin resistance markers were analysed in four groups: controls (n = 101); fasting hyperglycaemia (FH, n 45); impaired glucose tolerance; (IGT, n = 16) and those with features of both FH and IGT ('Both', n = 30). METHODS: Subjects underwent an OGTT. Plasma glucose, fasting lipid profiles, fasting, 30 and 120 min insulin were measured and beta cell function (% B) and insulin sensitivity (% S) assessed by homeostatic model assessment (HOMA) RESULTS: The FH group compared to controls had a significantly lower % B. The IGT group compared to controls had features of insulin resistance (higher body mass index (BMI), systolic blood pressure and 2 h insulin concentration). Subjects with 'both' IGT and FH had features of insulin resistance (higher BMI, systolic and diastolic blood pressure and triglyceride concentration) as well as beta cell dysfunction with a lower % B and 30 min insulin-glucose ratio compared to controls. There was a preponderance of males in this group. In all, 192 subjects' 30-min insulin concentration and incremental insulin response showed only a significantly negative correlation with fasting glucose concentration. In a linear regression analysis, a low 30-min insulin-glucose ratio was only a significant factor in the fasting glucose model. Thus, higher fasting glucose concentrations appear to be associated with beta cell dysfunction. However, HbA1 only showed a significant correlation with 120-min glucose, not fasting glucose concentration. CONCLUSIONS: In those with milder degrees of glucose intolerance, FH is associated with beta cell dysfunction and those with IGT and a relatively 'normal' fasting glucose have features of the insulin resistance syndrome.     

Gender differences in the prevalence of impaired fasting glycaemia and impaired glucose tolerance in Mauritius. Does sex matter?

OBJECTIVE: To examine gender differences in the characteristics and prevalence of various categories of glucose tolerance in a population study in Mauritius. RESEARCH DESIGN AND METHODS: In 1998, a community-based cross-sectional survey was conducted in Mauritius. Categories of glucose metabolism were determined in 5388 adults, with an oral glucose tolerance test given to those who did not have previously diagnosed diabetes (n=4036). Other cardiovascular risk factors were assessed among those without known diabetes. RESULTS: For men and women the prevalence of diabetes (22.0 vs. 21.8%, respectively) and the prevalence of coexisting impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) (3.2 vs. 2.9%) were similar. However, men were twice as likely as women to have isolated IFG [5.1% (4.2-6.0) vs. 2.9% (2.3-3.5)], despite being younger, thinner and with lower plasma insulin but higher lipids. Conversely, the prevalence of isolated IGT was lower in men [9.0% (7.9-10.2) vs. 13.9% (12.6-15.1)]. Among non-diabetic individuals, fasting glucose was higher in men than women, whereas 2-h glucose was higher in women. In people without diabetes, women had significantly higher body mass index, beta cell function (HOMA-B), fasting and 2-h insulin than men and significantly lower waist-hip ratios, waist circumference, insulin sensitivity (HOMA-S) and triglycerides. CONCLUSION: In Mauritius, the distribution of impaired glucose metabolism differs by sex. The observation that IFG is more prevalent in men and IGT more prevalent in women raises important questions about their underlying aetiology and the ability of the current glucose thresholds to equally identify men and women at high-risk of developing diabetes. IFG should be seen as a complimentary category of abnormal glucose tolerance, rather than a replacement for IGT.